Serotonin Transporter Gene Polymorphism and Myocardial Infarction Etude Cas-Témoins de l’Infarctus du Myocarde (ECTIM)

• Published in: Circulation (New York, N.Y.) Vol. 105; no. 25; pp. 2943 - 2945
• Main Authors: Fumeron, Frédéric, Betoulle, Dina, Nicaud, Viviane, Evans, Alun, Kee, Frank, Ruidavets, Jean-Bernard, Arveiler, Dominique, Luc, Gérald, Cambien, François
• Format: Journal Article
• Language: English
• Published: 25.06.2002
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.CIR.0000022603.92986.99

Background — Depression is a risk factor for myocardial infarction (MI). Selective serotonin reuptake inhibitors reduce this risk. The site of action is the serotonin transporter (SLC6A4), which is expressed in brain and blood cells. A functional polymorphism in the promoter region of the SLC6A4 gene has been described. This polymorphism may be associated with the risk of MI. Methods and Results — The SLC6A4 polymorphism has been investigated by polymerase chain reaction in 671 male patients with MI and in 688 controls from the Etude Cas-Témoins de l’Infarctus du Myocarde (ECTIM) multicentric study. Percentages for LL, LS, and SS genotypes were 35.5%, 45.4%, and 19.1%, respectively, for cases versus 28.1%, 49.1%, and 22.8%, respectively, for controls. S allele frequency was 41.8% and 47.4% for cases and controls, respectively. After adjustment for age and center by using multivariable logistic regression, the odds ratio for MI associated with the LL genotype was 1.40 (95% CI 1.11 to 1.76, P =0.0047). Conclusions — The LL genotype of the SLC6A4 polymorphism is associated with a higher risk of MI. This could be attributable to the effect of the polymorphism on serotonin-mediated platelet activation or smooth muscle cell proliferation or on other risk factors, such as depression or response to stress.